The present invention relates to the non-invasive magnetic imaging of anatomic tissue structures in isolation from surrounding tissues, and, in particular, to the non-invasive magnetic imaging of nerve tissues. The present invention more specifically relates to the non-invasive quantitative measurement of damage to nerve tissue, such as the damage that occurs upon compression.
Clinically it is possible to estimate which neural pathway is involved in trauma by determining the end result loss of motor function and either abberant sensory function or complete loss of it. It is very difficult to determine where the lesion is and to what extent it has caused deterioration of the nerves involved.
Peripheral nerves are compound structures. Each nerve trunk consists of a very large number of nerve “fibers” (neurites) that are protoplasmic extensions of neuronal cell bodies located in the dorsal root ganglia (sensory neurons) and ventral horn of the spinal cord (motor neurons). All nerve fibers (except fine pain fibers) are surrounded by a fatty sheath of myelin which serves to enhance nerve impulse conduction (neural flow). The nerve fibers are grouped into fasciculi, bundles of fibers bound together by a fine connective tissue membrane (epineureum). The bundles of fasciculi comprising the nerve trunk are bound by a thicker membrane, the perineureum. The nerve trunk may be surrounded by other layers of protective connective tissue or fat.
Neuropathy in peripheral nerves may occur through the agency of traumatic distortion, including compression, stretch and breakage, and/or associated ischemia. The trauma may be acute, especially when the surrounding tissues are injured, or it may be chronic, and due to pathologic mechanical relations between the nerve and surrounding tissues: regional compression is considered to be the principal etiology in entrapment syndromes. There is rapid recovery from transient compression, but prolonged compression extends the recovery period because the nerve fibers are damaged. Remyelination and re-establishment of conduction must take place. Chronic and repetitive compression prevents recovery and results in severe neurologic impairment.
In chronic and repetitive compressions, which are more common than acute compressions, the damage is more extensive. Nerve trunks become thinned at the site of the compression, but may swell proximally. Characteristically conduction is slowed and conduction blocks occur as long segments of myelin are damaged. Depending on the severity of the chronic compression, the nerve trunk proximally will contain a full complement of myelinated fibers within its fasciculi; but at the level of compression and distally the number of myelinated fibers may be reduced significantly. The relative density of the myelinated fibers between proximal and distal portions of the nerve is a measure of loss of neurophysiologic function in its distal distribution.
Although nerve damage can occur anywhere within the body, some nerves are predisposed to chronic damage because of their structural relationships with other tissues. Classic sites for chronic nerve compression include the brachial plexus—especially where the cords of the plexus pass between the rib cage and clavicle, the elbow—where the ulna nerve winds around the olecranon process of the ulna bone, the carpal tunnel—where the median nerve lies between deep flexor tendons and the flexor retinaculum, the sacro-iliac region—where the lumbo-sacral trunk and sacral plexus lie on the bony surfaces of the pelvis, the gluteal region—where the sciatic nerve passes between the powerful gluteal musculature, the neck of the fibula—where the common peroneal nerve winds about the external surface of the bone, and the tarsal canal—where the tibial nerve winds beneath the tarsal bones to enter the sale of the foot.
Some nerves are vulnerable to acute trauma as a result of their intimate relationship to bones subject to fracture. These include that portion of the brachial plexus lying beneath the clavicle, the radial nerve—which winds about the shaft of the humerus, and the common peroneal nerve, which winds about the neck of the fibula.
Carpal Tunnel Syndrome (CTS) is defined as a pathologic condition in which the tunnel size is reduced, causing pressure on the median nerve with resultant pain and slight sensory impairment in the digits supplied by the nerve, and sometimes accompanied by slight wasting of the thenar muscles. The carpal groove is a deep concavity on the palmar surface of the carpus formed by lateral and medial projections of the carpal bones. The medial projection is formed by the pisi-form bone and the hamulus—a hook-like projection of the hamate bone. The lateral projection is formed by the tubercles of the scaphoid and trapezium bones. The carpal groove is converted into an osteofibrous carpal tunnel by a strong fibrous retinaculum attached to the lateral and medial margins of the carpal groove. The carpal tunnel transmits the tendons of the deep and superficial digital flexor muscles which in this region form a firm bundle.
The median nerve lies within the tunnel between the flexor retinaculum and the flexor tendon bundle. It emerges from behind the flexor digitorum superficialis distally in the forearm about 5 cm proximal to the flexor retinaculum of the carpus. It lies superficial to the deep digital flexor tendons and between the tendons of the superficial flexor muscle and the flexor carpi radialis. The nerve then passes deep to the flexor retinaculum of the wrist where normally it lies superficial to the stout bundle of flexor tendons.
Overt morphology associated with CTS includes carpal dislocations, carpal arthritis and tenosynovitis of the long flexor tendons. These conditions clearly restrict the space within the tunnel. There is often no apparent morphologic cause for the syndrome, but as complete division of the flexor retinaculum results in relief from symptoms in most cases it is assumed that mechanical compression that is not obvious from the gross morphology of the tunnel or its contents causes ischemia or directly compresses the median nerve.
Clinical symptoms includes weakening of the thenar muscles, parasthesias of the lateral palm, thumb and first two fingers. Other symptoms may include stiffness of the wrist and some pain.
Clinical examination consists of identifying those symptoms known to be associated with nerve damage. The anatomic distribution of the branches of peripheral nerves is constant and well known. The distribution of abnormal sensation or inability to utilize one or more muscles is a sure indicator of which nerve is involved.
Electromyography is used as a supplement to clinical examination. The technique uses needle electrodes inserted into suspect muscle. The intensity of the potentials measured is an indirect measure of the level of muscle activity. Neural flow stimulation also involves the use of needle electrodes. The technique compares input and output values of electric potentials.
None of these diagnostic techniques definitively identifies the focus of the neuropathy. In most cases, if the examination and electromyographic results are typical of those associated with a particular syndrome, the focus of the neuropathy can be estimated with some certainty based on experience; but false positive diagnoses are relatively common and may lead to unnecessary surgery or incomplete relief of the symptoms. In addition, electromyography is a relatively complex technique requiring some expertise to obtain a satisfactory diagnosis. Furthermore, the use of needle electrodes is invasive, and may prove painful. This can lead to false readings or patient rejection of the study.
A further problem is experienced with clinical examinations. Numerous patients attempt to simulate symptomatology in order to qualify for insurance compensation. Identifying these patients using an essentially subjective examination is difficult and time consuming for the diagnostician.
Despite conflicting reports in the literature, there is no convincing evidence that nerve morphology viewed in unassisted two-dimensional magnetic images is a clinically practical means of obtaining information about histological degeneration and impaired neural flow. At present, CTS patients are not referred for magnetic imaging scans as a diagnostic procedure.